Art (California) on 01/19/2024

Given the proven benefits that nattokinase has shown in terms of reversing the trend of atherosclerosis in humans, its value needs to be weighed in comparison to Eliquis. Eliquis is an anticoagulant that has bleeding as a common side effect as discussed here :

https://www.drugs.com/eliquis.html#side-effects

Nattokinase can also thin the blood and dissolve blood clots as discussed here :

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5372539/#:~:text=Nattokinase is considered to be, blood and dissolving blood clots.

Here is a relevant quote :

' Nattokinase (NK), a potent blood-clot dissolving protein used for the treatment of cardiovascular diseases, is produced by the bacterium Bacillus subtilis during the fermentation of soybeans to produce Natto. NK has been extensively studied in Japan, Korea, and China. Recently, the fibrinolytic (anti-clotting) capacity of NK has been recognized by Western medicine. The National Science Foundation in the United States has investigated and evaluated the safety of NK. '

If your doctor is willing, he/she may temporarily allow you to stop Eliquis to test nattokinase or reduce your dose of Eliquis so you can use nattokinase simultaneously. The reason I am mentioning nattokinase to you is because I feel it is actually stopping CVD at its most common source, atherosclerosis. Whereas, Eliquis is mainly treating symptoms such as clotting and people can still have stroke while taking Eliquis as discussed in the following human study :

https://j-stroke.org/upload/pdf/jos-2021-02355.pdf

Here is a relevant study quote :

' A total of 651 patients (mean age, 72.5±8.7 years) received apixaban for a mean duration of 82.7±37.4 weeks. Fifty-three bleeding events occurred in 39 patients (6.0%), and 10 (1.5%) experienced major bleeding. Seventeen patients (2.6%) had major events (stroke, n=15, 2.3%; all ischemic), systemic embolism (n=1, 0.2%), and death (n=3, 0.5%). MRI data showed no significant association between white matter ischemic changes and microbleeds, and major events or bleeding. Patients with cerebral atherosclerotic lesions had a higher rate of major events than those without (4.6% [n=10/219] vs. 1.7% [n=7/409], P=0.0357), which partly explains the increased prevalence of major outcomes in this group versus patients without stroke (0.7%, P=0.0002).'

See if you can find data suggesting that Eliquis can change the trend of atherosclerosis, which is usually the underlying problem. To give you an idea of what I am talking about, look at this study using just grape seed proanthocyanidin (GSPE) :

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4554789/

Here is a relevant study quote :

' As anticipated, after treatment, GSPE resulted in significant reduction in MMCIMT progression (4.2% decrease after six months, 4.9% decrease after 12 months and 5.8% decrease after 24 months) and plaque score (10.9% decrease after six months, 24.1% decrease after 12 months and 33.1% decrease after 24 months) for the primary outcome, while MMCIMT and plaque score were stable and even increased with the time going on in control group. The number of plaques and unstable plaques also decreased after treatment of GSPE. Furthermore, the carotid plaque can disappear after treatment with GSPE. The incidence rate for transitory ischemic attack (TIA), arterial revascularization procedure, and hospital readmission for unstable angina in GSPE group were statistically significant lower (P = 0.02, 0.08, 0.002, respectively) compared with the control group. '

Here is a graph that gives a great visual representation of what this relatively low dose of GSPE did in this study to significantly alter the atherosclerotic trend from upward to downward :

If Eliquis could produce these same effects as GSPE while acting as an anticoagulant, that would be useful, but I can't find any data that shows that it does. If you can find such data, please share it with me. This is a major reason why I use GSPE myself. It is also worth mentioning that while GSPE can have a significant effect on on carotid plaque and plaque score, its effects on cholesterol levels are minimal.

Doctors will tell you that statins can help atherosclerosis, but statins mainly slow progression of atherosclerosis. Statins only reduce the chance of having a heart attack by 25% to 35% as discussed in this Harvard article :

https://www.health.harvard.edu/heart-health/one-in-five-people-at-risk-of-heart-disease-shuns-statins#:~:text=Cholesterol-lowering statins can reduce, common, life-threatening events.

Here is a relevant quote from the article :

' Cholesterol-lowering statins can reduce the odds of having a heart attack by about 25% to 35%, especially in people at high risk for these common, life-threatening events. '

That means that 65% to 75% of people taking statins still have the potential for a heart attack.

I believe that cholesterol is a poor marker for atherosclerosis because many people with good cholesterol levels still have heart attacks as discussed here :

https://www.cardiosmart.org/news/2017/12/half-of-patients-with-ideal-cholesterol-have-underlying-heart-risks#:~:text=Optimal cholesterol levels don't, build-up in their arteries.

Here is a relevant article quote :

' Optimal cholesterol levels don’t always translate to perfect heart health, based on a recent study that found half of healthy patients with normal cholesterol levels have dangerous plaque build-up in their arteries. '

Altering the atherosclerosis trend from upward to downward makes sense since atherosclerosis is the dominant cause of cardiovascular disease which includes strokes and heart attacks among others. Cholesterol does not seem to be a great marker for atherosclerosis, but atherosclerosis is a very good marker for CVD.

Art